Yours is not the same as mine

Hasson T, Kolitz S, Towfic F, Laifenfeld D, Bakshi S, Beriozkin O, Shacham-Abramson M, Timan B, Fowler KD, Birnberg T, Konya A, Komlosh A, Ladkani D, Hayden MR, Zeskind B, Grossman I.
Functional effects of the antigen glatiramer acetate are complex and tightly associated with its composition. J Neuroimmunol. 2016;290:84-95. doi: 10.1016/j.jneuroim.2015.11.020

Glatiramer acetate (Copaxone®; GA) is a non-biological complex drug for multiple sclerosis. GA modulated thousands of genes in genome-wide expression studies conducted in THP-1 cells and mouse splenocytes. Comparing GA with differently-manufactured glatiramoid Polimunol (Synthon) in mice yielded hundreds of differentially expressed probesets, including biologically-relevant genes (e.g. Il18, adj p<9e-6) and pathways. In human monocytes, 700+ probesets differed between Polimunol and GA, enriching for 130+ pathways including response to lipopolysaccharide (adj. p<0.006). Key differences were confirmed by qRT-PCR (splenocytes) or proteomics (THP-1). These studies demonstrate the complexity of GA’s mechanisms of action, and may help inform therapeutic equivalence assessment.

How do you get brand loyalty, by showing your brand is better or if the you are already the market leader show that you are different from the competitor. This study by Teva/Teva associates does just that by showing the the genes expressed after Polimunol (Glateriamer me-too) are not quite the same. So are you going to try something that is different. However they have done a  trial and it has similar efficacy.

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  • If gene expression profile is different for GA me-too, but efficacy is the same, it seems to imply that differentially expressed genes are irrelevant. So – perhaps a way to narrow down how GA does NOT work?

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